Summary: New research shows that blood from older animals can speed up Alzheimer’s-related changes in the brain, while young blood may slow them down. In a long-term experiment, mice engineered to develop Alzheimer’s symptoms received weekly blood infusions from either young or old donors.
Older blood increased amyloid buildup and worsened cognitive performance, while young blood appeared to have protective effects. Proteomic analysis revealed more than 250 altered proteins linked to synaptic signaling, calcium channels, and other pathways tied to neurodegeneration. The findings highlight circulating blood factors as potential targets for future Alzheimer’s therapies.
Key Facts
- Blood-Borne Influence: Aged blood accelerated amyloid buildup and cognitive decline in Alzheimer’s-model mice.
- Protective Effect: Young blood altered brain protein profiles in ways consistent with improved synaptic and neuronal function.
- Therapeutic Potential: Results point to blood-derived factors as a new frontier for Alzheimer’s interventions.
Source: Melisa Institute
Alzheimer’s disease is the most common form of dementia worldwide and continues to be one of the greatest public health challenges.
New research, published in the journal Aging-US, reveals that blood from aged mice can accelerate the progression of the disease, while young blood may have protective effects.
The study was led by researchers from Instituto Latinoamericano de Salud Cerebral (BrainLat) at Universidad Adolfo Ibáñez in conjunction with MELISA Institute, the University of Texas Health Science Center at Houston, and Universidad Mayor.
Alzheimer’s is characterized by the abnormal accumulation of beta-amyloid protein (Aβ) in the brain, forming plaques that disrupt communication between neurons and generate neurodegenerative processes.
Although this protein originates in the central nervous system, recent studies have suggested that it may also be present in the blood, opening new possibilities for understanding how the disease progresses.
To explore this hypothesis, the team used Tg2576 transgenic mice (a model widely used in Alzheimer’s research), which received weekly blood infusions from young and old mice for 30 weeks to assess whether factors present in the blood could modulate amyloid accumulation and the animals’ behavior.
“This collaborative work between various institutions reinforces the importance of understanding how systemic factors condition the brain environment and directly impact mechanisms that promote disease progression.
By demonstrating that peripheral signals derived from aged blood can modulate central processes in the pathophysiology of Alzheimer’s, these findings open new opportunities to study therapeutic targets aimed at the blood-brain axis,” explained Dr. Claudia Durán-Aniotz, from the Instituto Latinoamericano de Salud Cerebral (BrainLat) at Universidad Adolfo Ibáñez.
The team assessed cognitive performance using the Barnes test, the accumulation of amyloid plaques with histological and biochemical techniques, and performed a comprehensive proteomic analysis of the treated brains.
This analysis revealed more than 250 differentially expressed proteins, linked to synaptic functions, endocannabinoid signaling, and calcium channels, which could explain the observed changes.
Regarding MELISA Institute’s participation in this research, Mauricio Hernández, a proteomics expert at the research and biotechnology center, commented that “within this study, we conducted a large-scale proteomic analysis that allowed us to generate excellent quality data in this complex matrix like plasma, a technical challenge for any proteomics laboratory. Thanks to our state-of-the-art equipment (timsTOF Pro2), we are proud to have contributed to the production of a robust and high-quality scientific article.”
These results reinforce the idea that circulating factors in the blood can directly influence the progression of neurodegenerative diseases such as Alzheimer’s. Understanding these mechanisms will allow for the identification of new therapeutic targets and preventative strategies. The next step will be to determine exactly what these factors are and whether it is possible to intervene in them in humans.
“It is a pleasure to contribute our proteomic capabilities to support innovative research initiatives like this study, which allow us to advance the knowledge and development of new therapies for neurodegenerative diseases, which are currently a global health problem,” emphasized Dr. Elard Koch, Chairman of MELISA Institute.
Funding:
C.DA. was supported by ANID/FONDECYT Regular 1210622, ANID/PIA/ANILLOS ACT210096, the Alzheimer’s Association (AARGD-24-1310017), ANID/FOVI240065 and ANID/Proyecto Exploracion 13240170 and MULTI-PARTNER CONSORTIUM TO EXPAND DEMENTIA RESEARCH IN LATIN AMERICA (ReDLat), supported by NIH research grant R01AG057234 funded by the National Institute of Aging (NIA) and the Fogarty International Center (FIC), an Alzheimer’s Association grant (SG-20-725707-ReDLat), the Rainwater Charitable Foundation, and the Global Brain Health Institute with additional support from the Bluefield Project to Cure Frontotemporal Dementia, an NIH contract (75NS95022C00031), and NIA under awards R01AG075775, R01AG082056, and R01AG083799.
The content is solely the responsibility of the authors and does not represent the official views of the National Institutes of Health, the Alzheimer’s Association, Rainwater Charitable Foundation, Bluefield Project to Cure Frontotemporal Dementia, or the Global Brain Health Institute.
The contribution of RM and team in this work was supported by NIH grants RF1AG072491 and RF1AG059321. UW was supported by ANID/FONDECYT Regular 1240176.
Key Questions Answered:
A: Mice that received blood from older donors showed faster amyloid plaque accumulation, altered brain protein profiles, and worse performance on cognitive tests. These changes suggest that circulating factors in aged blood actively promote processes linked to Alzheimer’s progression.
A: Young blood shifted brain protein expression toward patterns associated with healthier synaptic signaling and reduced disease-related dysfunction. These protective effects point to specific molecular factors that may slow or counteract neurodegeneration.
A: The findings reveal that the blood–brain axis plays a meaningful role in driving or slowing Alzheimer’s progression. Identifying the exact blood-borne molecules involved could lead to new therapeutic targets or preventative strategies aimed at modifying systemic factors rather than the brain alone.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this Alzheimer’s disease research news
Author: Damian Vallejos
Source: Melisa Institute
Contact: Damian Vallejos – Melisa Institute
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Infusion of blood from young and old mice modulates amyloid pathology” by Claudia Durán-Aniotz et al. Aging-US
Abstract
Infusion of blood from young and old mice modulates amyloid pathology
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the accumulation of misfolded proteins in the brain.
Recently, the impact of blood components in the progression of this disease has come to attention.
This study investigates the effects of infusing blood from young and old wild-type mice into transgenic mice that model AD brain amyloidosis.
Impaired memory and Aβ accumulation were observed in mice infused with blood from old donors.
A proteomic analysis in the brain of these mice identified alterations in components related to synaptogenesis and the endocannabinoid system. The α2δ2 protein, associated with neuronal calcium regulation, was validated as a possible mediator of the observed effects.
This study highlights the influence of blood in AD pathology and the identification of potential therapeutic targets.
